Melatonin supplementation does not alter vascular function or oxidative stress in healthy normotensive adults on a high sodium diet.

High sodium diets (HSD) can cause vascular dysfunction, in part due to increases in reactive oxygen species (ROS). Melatonin reduces ROS in healthy and clinical populations and may improve vascular function. The purpose was to determine the effect of melatonin supplementation on vascular function and ROS during 10 days of a HSD. We hypothesized that melatonin supplementation during a HSD would improve vascular function and decrease ROS levels compared to HSD alone. Twenty-seven participants (13 M/14 W, 26.7 ± 2.9 years, BMI: 23.6 ± 2.0 kg/m2 , BP: 110 ± 9/67 ± 7 mmHg) were randomized to a 10-day HSD (6900 mg sodium/d) supplemented with either 10 mg of melatonin (HSD + MEL) or a placebo (HSD + PL) daily. Brachial artery flow-mediated dilation, a measure of macrovascular function, (HSD + PL: 7.1 ± 3.8%; HSD + MEL: 6.7 ± 3.4%; p = 0.59) and tissue oxygenation index (TSI) reperfusion rate, a measure of microvascular reactivity, (HSD + PL: 0.21 ± 0.06%/s; HSD + MEL: 0.21 ± 0.08%/s; p = 0.97) and TSI area under the curve (HSD + PL: 199899 ± 10,863 a.u.; HSD + MEL: 20315 ± 11,348 a.u.; p = 0.17) were similar at the end of each condition. Neither nitroxide molarity (HSD + PL: 7.8 × 10-5 ± 4.1 × 10-5 mol/L; HSD + MEL: 8.7 × 10-5 ± 5.1 × 10-5 mol/L; p = 0.55) nor free radical number (HSD + PL: 8.0 × 1015 ± 4.4 × 1015 ; HSD + MEL: 9.0 × 1015 ± 4.9 × 1015 ; p = 0.51) were different between conditions. Melatonin supplementation did not alter vascular function or ROS levels while on a HSD in this sample of young healthy normotensive adults.

Melatonin supplementation reduces nighttime blood pressure but does not affect blood pressure reactivity in normotensive adults on a high-sodium diet.

High-sodium diets (HSDs) can cause exaggerated increases in blood pressure (BP) during physiological perturbations that cause sympathetic activation, which is related to cardiovascular risk. Melatonin supplementation has been shown to play a role in BP regulation. Our aim was to examine the effects of melatonin taken during an HSD on 24-h BP and BP reactivity during isometric handgrip (IHG) exercise, postexercise ischemia (PEI), and the cold pressor test (CPT). Twenty-two participants (11 men/11 women, 26.5 ± 3.1 yr, BMI: 24.1 ± 1.8 kg/m2, BP: 111 ± 9/67 ± 7 mmHg) were randomized to a 10-day HSD (6,900 mg sodium/day) that was supplemented with either 10 mg/day of melatonin (HSD + MEL) or placebo (HSD + PL). Twenty-four-hour ambulatory BP monitoring was assessed starting on day 9. Mean arterial pressure (MAP) was quantified during the last 30 s of IHG at 40% of maximal voluntary contraction and CPT, and during 3 min of PEI. Melatonin did not change 24-h MAP (HSD + PL: 83 ± 6 mmHg; HSD + MEL: 82 ± 5 mmHg; P = 0.23) but decreased nighttime peripheral (HSD + PL: 105 ± 10 mmHg; HSD + MEL: 100 ± 10 mmHg; P = 0.01) and central systolic BP (HSD + PL: 97 ± 9 mmHg; HSD + MEL: 93 ± 8 mmHg; P = 0.04) on the HSD compared with the HSD + PL. The absolute and percent change in MAP during IHG was not different between conditions (all P > 0.05). In conclusion, melatonin supplementation did not alter BP reactivity to the perturbations tested on an HSD but may be beneficial in lowering BP in young healthy normotensive adults.NEW & NOTEWORTHY BP reactivity was assessed during isometric handgrip (IHG) exercise, postexercise ischemia (PEI), and the cold pressor test (CPT) after 10 days of a high-sodium diet with and without melatonin supplementation. Melatonin did not alter BP reactivity in healthy normotensive men and women. However, melatonin did decrease nighttime peripheral and central systolic BP, suggesting it may be beneficial in lowering BP even in those with a normal BP.

Greater adherence to healthy dietary patterns is associated with lower diastolic blood pressure and augmentation index in healthy, young adults.

More than two-thirds of cardiovascular disease (CVD) deaths worldwide are attributable to dietary factors. Blood pressure variability (BPV), endothelial dysfunction, and arterial stiffness are important CVD risk factors. Although studies show a link between consuming a healthy diet and lower BPV and stiffness and improved endothelial function, research in young, healthy adults is scarce. We hypothesized that, in young, healthy adults, diet quality would be inversely associated with BPV and arterial stiffness and positively associated with endothelial function. This cross-sectional study included 56 healthy young adults (34 women/22 men, age 26.7 ± 0.8 years, body mass index 23.4 ± 0.4 kg/m2, blood pressure [BP] 113/69 mmHg). Three-day diet records were used to calculate two Dietary Approaches to Stop Hypertension (DASH) diet scores, the alternative Mediterranean Diet (aMED) score, and the Healthy Eating Index-2015 (HEI-2015) based on the 2015-2020 Dietary Guidelines for Americans. Twenty-four-hour ambulatory BP data were used to calculate average real variability of systolic and diastolic BP. Endothelial function was assessed by flow-mediated dilation, and arterial stiffness was assessed by pulse wave velocity and augmentation index (AIx). Overall, the HEI-2015 was inversely associated with 24-hour diastolic BP (DBP) and daytime DBP, and the aMED score was inversely associated with AIx. In our exploratory analyses, the Fung DASH score was inversely associated with 24-hour DBP and daytime DBP in women, but not men. These findings suggest that consuming a diet that aligns with the DASH diet, the Mediterranean diet, and/or the 2015-2020 Dietary Guidelines for Americans is associated with cardiovascular benefits in healthy, young adults.

Arterial Stiffness and Endothelial Function are Comparable in Young Healthy Vegetarians and Omnivores.

Vegetarians (VEG) are reported to have lower body weight, blood pressure (BP), and cardiovascular disease (CVD) risk compared with omnivores (OMN), yet the mechanisms remain unclear. A vegetarian diet may protect the vascular endothelium, reducing the risk of atherosclerosis and CVD. This cross-sectional study compared vascular function between OMN and VEG. We hypothesized that VEG would have greater vascular function compared with OMN. Fifty-eight normotensive young healthy adults participated (40 women [W]/18 men [M]; 28 OMN [15W/13M] and 30 VEG [25W/5M]; 26 ± 7 years; BP: 112 ± 11/67 ± 8 mm Hg). Arterial stiffness, assessed by carotid-to-femoral pulse wave velocity (OMN: 5.6 ± 0.8 m/s, VEG: 5.3 ± 0.8 m/s; P = .17) and wave reflection assessed by aortic augmentation index (OMN: 6.9 ± 12.3%, VEG: 8.8 ± 13.5%; P = .57) were not different between groups. However, central pulse pressure (OMN: 32 ± 5; VEG: 29 ± 5 mm Hg; P = .048) and forward wave reflection were greater in omnivores (OMN: 26 ± 3; VEG: 24 ± 3 mm Hg; P = .048). Endothelial-dependent dilation measured by brachial artery flow-mediated dilation was not different between groups (OMN: 6.0 ± 2.9%, VEG: 6.9 ± 3.3%; P = .29). Percent change in femoral blood flow from baseline during passive leg movement, another assessment of nitric oxide-mediated endothelial dilation, was similar between groups (OMN: 203 ± 88 mL/min, VEG: 253 ± 192 mL/min; P = .50). These data suggest that in healthy young adults, normotensive VEG do not have significantly improved vascular function compared with OMN; however, they have a lower central pulse pressure and forward wave amplitude which may lower the risk of future CVD.